Evidence map›Paper›PMID 29573323›Full record

ArticleGenes, brain, and behavior2018

The interaction of the Chrna5 D398N variant with developmental nicotine exposure.

H C O'Neill, C R Wageman, S E Sherman, S R Grady, M J Marks, J A Stitzel

Open access · greenAbstract read
In one paragraph

Article in Genes, brain, and behavior, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 pooled it
0.9field-weighted citation impact, top 26% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

9 citing papers in PubMed, 1 synthesis or guideline pooled it, 14 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Little Evidence of Modified Genetic Effect of rs16969968 on Heavy Smoking Based on Age of Onset of Smoking.Nicotine & tobacco research : official journal of the Society for Research on Nicotine and Tobacco · 2021
    Article
  6. Review
  7. Article
  8. The Role of A Priori-Identified Addiction and Smoking Gene Sets in Smoking Behaviors.Nicotine & tobacco research : official journal of the Society for Research on Nicotine and Tobacco · 2020
    Article
  9. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

H C O'NeillInstitute for Behavioral Genetics, University of Colorado, Boulder, Colorado.ORCID 0000-0001-7250-1494
C R WagemanInstitute for Behavioral Genetics, University of Colorado, Boulder, Colorado.
S E ShermanInstitute for Behavioral Genetics, University of Colorado, Boulder, Colorado.
S R GradyInstitute for Behavioral Genetics, University of Colorado, Boulder, Colorado.
M J MarksInstitute for Behavioral Genetics, University of Colorado, Boulder, Colorado.
J A StitzelInstitute for Behavioral Genetics, University of Colorado, Boulder, Colorado.
University of Colorado Boulder · US

Funding

Role of Chrna5 genotype on outcomes of developmental nicotine exposureR21DA040228 · NIDA · UNIVERSITY OF COLORADO · PI STITZEL, JERRY A · 2015 to 2016
$414k
NIDA NIH HHS R21 DA040228NIDA NIH HHS R21DA040228
6 · The paper itself

Abstract

A single nucleotide polymorphism (SNP) in CHRNA5 (rs16969968, change from an aspartic acid [D] to asparagine [N] at position 398 of the human α5 nicotinic acetylcholine receptor subunit) has been associated with increased risk for nicotine dependence. Consequently, carriers of the risk variant may be at elevated risk for in utero nicotine exposure. To assess whether this gene-environment interaction might impact nicotine intake in developmental nicotine-exposed offspring, we utilized a mouse expressing this human SNP. D and N dams drank nicotine (100 μg/mL) in 0.2% saccharin water or 0.2% saccharin water alone (vehicle) as their sole source of fluid from 30 days prior to breeding until weaning of offspring. The nicotine (D Nic, N Nic) or vehicle (D Veh, N Veh) exposed offspring underwent a 2-bottle choice test between postnatal ages of 30 to 46 days. N Nic offspring consumed the most nicotine at the highest concentration (400 μg/mL) compared with all other groups. In contrast, D Nic offspring drank the least amount of nicotine at all concentrations tested. Nicotine-stimulated dopamine (DA) release measured from striatal synaptosomes was increased in D Nic offspring, while decreased in N Nic offspring relative to their genotype-matched controls. These data suggest that the α5 variant influences the effect of developmental nicotine exposure on nicotine intake of exposed offspring. This gene-environment interaction on striatal DA release may provide motivation for increased nicotine seeking in N Nic offspring and reduced consumption in D Nic offspring.

Indexed as

AnimalsDisease Models, AnimalFemaleGene-Environment InteractionMaleMiceMice, TransgenicNicotinePolymorphism, Single NucleotidePregnancyPrenatal Exposure Delayed EffectsReceptors, NicotinicTobacco Use DisorderCHRNA5 protein, mouseNicotineReceptors, Nicotinicadolescent nicotineCHRNA5D398N mousedevelopmentdopaminegene by environment interactionnicotinenicotine dependencenicotinic receptorsrs16969968

Identifiers

PMID29573323
PMCPMC7313682
OpenAlexW2790344023

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.